:Homocysteine:

Function: risk factor for cardiovascular disease, much more significant than cholesterol.

Homocystine is a natural amino acid metabolite of the essential amino acid methionine, but it occurs only transiently before being converted to the harmless cystathionine via a vitamin B6-dependent enzyme. Homocystine is the double-bonded form of homocysteine. Homocysteine metabolism is related to sulfur amino acid metabolism (methionine, taurine and cysteine) and is dependent on vitamin B12, folic acid, vitamin B6 and betaine as primary cofactors. Homocysteine metabolism is relevant to the understanding of psychosis, arteriosclerosis and the biochemical basis of all nutrient therapies.

Homocysteine excess is still another metabolic cause of psychosis and mental retardation. Nutrients-vitamin B6, folic acid, betaine, cysteine and vitamin B12 can help various inborn errors of homocysteine metabolism. There is a similar form of psychosis, called pyroluria, which accounts for about 30% of psychotic patients (Pfeiffer, 1975). These patients are vitamin B6 and zinc dependent.

S-adenosyl homocysteine can be a useful therapy in certain forms of psychosis. Homocysteine, which presumably accumulates as a result of insufficient vitamin B6, is identified as a chief culprit in initiating the vascular lesions leading to arteriolosclerosis. Zinc deficiency also may have a role in this process. With this knowledge, the nutrient basis of heart disease prevention is expanded beyond the simplistic theory related to cholesterol and the restricted consumption of eggs. Beyond the treatment of arteriosclerosis by reduction of cholesterol is treatment by reduction of homocystine. Homocystine excess is related to deficiency of vitamin B6 and other methyl donors as well as zinc deficiency, which has a role in the body's ability to repair cells. Marginal deficiency of vitamin B6 and zinc is widespread in this country (Pfeiffer, 1975).